EPSP amplitude modulation at the rat Ia-alpha motoneuron synapse: Effects
of GABA-B receptor agonists and antagonists.
Kavita R. Peshori, William F. Collins, III and Lorne M. Mendell.
Department of Neurobiology and Behavior, State University of New York at
Stony Brook, Stony Brook, N.Y. 11794-5230.
APStracts 4:237N, 1997.
ABSTRACT
The object of this study was to examine the relationship between EPSP
amplitude, post tetanic potentiation and EPSP amplitude modulation at synapses
made by group Ia afferents on motoneurons in the rat. These relationships were
evaluated in cells in untreated rats and in cells in rats treated with the
GABA-B receptor agonist baclofen and antagonist CGP-35348 which were used to
manipulate Ca++ entry into presynaptic terminals and consequently probability
of transmitter release from them. There was no evidence for postsynaptic
action of these drugs from measurement of their effects on motoneuron
properties. During high frequency stimulation (32 shock bursts at 167 Hz),
EPSP amplitude either decreased (negative modulation) or increased (positive
modulation) in response to successive stimuli at different connections. In
untreated rats this frequency-dependent amplitude modulation behavior was
inversely but weakly correlated with EPSP amplitude measured at low frequency.
Intravenous (i.v.) administration of the GABA-B agonist, baclofen, produced a
marked and progressive decrease in EPSP amplitude measured at low frequency
coincident with a change in frequency-dependent EPSP amplitude modulation
towards more positive values (synaptic facilitation). In contrast, an increase
in EPSP amplitude occurred following i.v. administration of the GABA-B
antagonist CGP-35348 that was accompanied by a negative shift in EPSP
amplitude modulation during high frequency stimulation. The negative shift in
EPSP amplitude modulation (synaptic depression) following CGP-35348
application was much smaller than the positive shift induced by baclofen when
normalized to the change in EPSP amplitude. Post tetanic potentiation
decreased after baclofen but did not increase after CGP-35348. The
relationship between modulation and EPSP amplitude was much steeper after
GABA-B receptor manipulation in either direction than that observed in the
population of motoneurons in untreated preparations. This suggests that in the
rat differences in probability of release play at most a small role in
determining EPSP amplitude across the motoneuron pool.
Received 2 July 1997; accepted in final form 4 September 1997.
APS Manuscript Number J556-7.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 7 October 1997